The effects of unsaturated fatty acids on Helicobacter pylori in vitro

Khulusi, S.; Ahmed, H. A.; Patel, Praful; Mendall, Michael A.; Northfield, T. C.

doi:10.1099/00222615-42-4-276

Cited by 63 publications

(49 citation statements)

References 31 publications

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“…Higher Levels of Lipid Hydroperoxides in ahpC Mutant Cells-Unsaturated fatty acids have been found repeatedly as a constituent of lipids in H. pylori, and the growth of H. pylori displays sensitivity to the addition of unsaturated free fatty acids because of their incorporation into phospholipids and subsequent membrane destruction (40,41). Thus, under the physiological (oxidative stress) condition, there might be a steady flow of lipid hydroperoxides present within H. pylori cells, a situation that would require an abundant organic peroxide reductase activity to remove the damaging organic hydroperoxides.…”

Section: Fig 2 Catalase Activities and The Epr Signals In Various Hmentioning

confidence: 99%

Role of a Bacterial Organic Hydroperoxide Detoxification System in Preventing Catalase Inactivation

Wang¹,

Conover

Benoit³

et al. 2004

Journal of Biological Chemistry

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In the gastric pathogen Helicobacter pylori, catalase (KatA) and alkyl hydroperoxide reductase (AhpC) are two highly abundant enzymes that are crucial for oxidative stress resistance and survival of the bacterium in the host. Here we report a connection unidentified previously between the two stress resistance enzymes. We observed that the catalase in ahpC mutant cells in comparison with the parent strain is inactivated partially (approximately 50%). The decrease of catalase activity is well correlated with the perturbation of the heme environment in catalase, as detected by electron paramagnetic resonance spectroscopy. To understand the reason for this catalase inactivation, we examined the inhibitory effects of hydroperoxides on H. pylori catalase (either present in cell extracts or added to the purified enzyme) by monitoring the enzyme activity and the EPR signal of catalase. H. pylori catalase is highly resistant to its own substrate, without the loss of enzyme activity by treatment with a molar ratio of 1:3000 H 2 O 2 . However, it is inactivated by lower concentrations of organic hydroperoxides (the substrate of AhpC). Treatment with a molar ratio of 1:400 t-butyl hydroperoxide resulted in an inactivation of catalase by approximately 50%. UV-visible absorption spectra indicated that the catalase inactivation by organic hydroperoxides is caused by the formation of a catalytically incompetent compound II species. To further support the idea that organic hydroperoxides, which accumulate in the ahpC mutant cells, are responsible for the inactivation of catalase, we compared the level of lipid peroxidation found in ahpC mutant cells with that found in wild type cells. The results showed that the total amount of extractable lipid hydroperoxides in the ahpC mutant cells is approximately three times that in the wild type cells. Our findings reveal a novel role of the organic hydroperoxide detoxification system in preventing catalase inactivation.

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Section: Fig 2 Catalase Activities and The Epr Signals In Various Hmentioning

confidence: 99%

Role of a Bacterial Organic Hydroperoxide Detoxification System in Preventing Catalase Inactivation

Wang¹,

Conover

Benoit³

et al. 2004

Journal of Biological Chemistry

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“…Interestingly, fatty acids can also be metabolized into various products which can also inhibit bacterial growth. For example, arachidonic acid, a fatty acid derived from linoleic acid [18] inhibited the growth of gram-positive bacteria such as Streptococcus faecalis, Staphylococcus epidermidis, S. aureus [19] and gram-negative H. pylore [20]. Moreover, arachidonic acid is a precursor to prostanoid synthesis when released from membrane phospholipids in response to various stimuli.…”

Section: Introductionmentioning

confidence: 99%

Effect of Prostaglandin F2ÃÂ± on Growth of Staphylococcus Aureus Associated with Bovine Mastitis

Autran¹

2013

J Veterinar Sci Technol

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Staphylococcus aureus is a major infectious organism causing mastitis. Certain fatty acids have been shown to inhibit the growth of pathogens including Staphylococcus aureus. An in vitro experiment was conducted to determine the effects of prostaglandin F 2α (PGF 2α ) on growth of S. aureus. Flasks containing tryptic soy broth (TSB) were inoculated with S. aureus Novel, and subsequently treated with PGF 2α (dinoprost tromethamine) at concentrations of 0, 0.3, 0.6, 1.2, and 2.4 mg/ml. Cultures were incubated at 37°C for 24 h and sampled every 3 h. The entire experiment was conducted three times in duplicates. Bacterial growth was assessed by counting colony forming units (CFU) in triplicates. Data were analyzed by repeated measures analysis of variance and reduced and full dummy variable regression models to determine the effect of PGF 2α concentrations on growth patterns of S. aureus over time. There was an effect of treatment and treatment by time interaction (P<0.05) on mean log CFU, indicating that bacterial growth over 24 h was different across treatments. At time of inoculation (0 h), mean log CFU values were not different among treatments; however at 24 h, mean log CFU for each PGF 2α treatment was different from control and decreased (P<0.05) with increasing concentrations of PGF 2α . The predicted growth curve for each treatment was different (P<0.05) when compared with the control, and the rate of bacterial growth was less for 1.2 mg/ml PGF 2α when compared with the control and 0.6 mg/ml. The bacterial growth was completely inhibited during the 24 h period in 2.4 mg/ml PGF 2α treatment. Furthermore, a non-linear regression model was employed to estimate the dose response at the 24 h, and revealed that 1.2 mg/ml was the minimum inhibitory dose. These results provide evidence, for the first time, that PGF 2α , in the form of dinoprost tromethamine, has bacteriostatic and bactericidal effects on S. aureus in vitro.

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“…Based on re cent results which dem onstrated prooxidant activ ity of structurally unrelated lipophils in E. coli, it is suggested that microbiocidal activity of lipophils may be exacerbated by superoxide, generated by autoxidation of respiratory reductants following membrane derangement. Organic compounds with unspecific microbiocidal activity include fatty acids (Khulusi et al, 1995), local and general anes thetics, antimalarial agents, the anti-gout drug pro benecid (4-[(dipropylamino)sulfonyl]benzoic acid), antihistamines, barbiturates, salicylates, diuretics, steroids, phenols, the anti-oxidants BHT and BHA (butylated hydroxytoluene and butylated hydroxyanisole), and other organic com pounds (Sikkema et al, 1995).…”

Section: Oxidant Toxicity Of Hydrocarbons and Xenobioticsmentioning

confidence: 99%

Common Solvent Toxicity: Autoxidation of Respiratory Redox-Cyclers Enforced by Membrane Derangement

Garbe

Yukawa

2001

Zeitschrift Für Naturforschung C

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Respiration, Lipophilicity, ProoxidantsUnspecific biological effects of chemically diverse solvents strikingly reveal the unifying motif of oxidant toxicity both in higher organisms and in aerobic bacteria. In a few spectacu lar cases, solvent metabolites with oxidant properties were dem onstrated, which however cannot explain extrahepatic toxicity, e.g. in muscle and nerve cells. A common source of solvent-inducible oxidants, by contrast, is suggested to be located in mitochondria or, more general, in m embranes where the respiratory chain operates. Orderly respiration depends on membrane integrity, which is invariably compromised by exposure to most solvents and many other lipophils. In rat mitochondria, toluene-induced membrane derangem ent has been di rectly implicated with superoxide production, resulting from autoxidation of the membranelocated respiratory redox-cycler ubisemiquinone. A related mechanism may occur in bacteria: Exposure of Escherichia coli to lipophils such as ethanol, tetralin, indole, chlorpromazine and procaine, or to heat shock, induces anti-oxidant proteins, which are reliable indicators of increased oxidant levels. Although many molecular details remain to be elucidated, this review documents that oxidant toxicity of lipophilic compounds is a common physiological phenom enon correlated with derangement of membranes where respiratory processes take place. Subjective consequences of acute oxidant injury are probably the hangover from alco hol and nicotine consumption, and the sudden death from recreational solvent abuse. Sugges tions concerning oxidants as major contributors to ageing remain unchallenged. T ren ds A r tic le -M in irev iew

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The effects of unsaturated fatty acids on Helicobacter pylori in vitro

Cited by 63 publications

References 31 publications

Role of a Bacterial Organic Hydroperoxide Detoxification System in Preventing Catalase Inactivation

Role of a Bacterial Organic Hydroperoxide Detoxification System in Preventing Catalase Inactivation

Effect of Prostaglandin F2ÃÂ± on Growth of Staphylococcus Aureus Associated with Bovine Mastitis

Common Solvent Toxicity: Autoxidation of Respiratory Redox-Cyclers Enforced by Membrane Derangement

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The effects of unsaturated fatty acids on Helicobacter pylori in vitro

Cited by 63 publications

References 31 publications

Role of a Bacterial Organic Hydroperoxide Detoxification System in Preventing Catalase Inactivation

Role of a Bacterial Organic Hydroperoxide Detoxification System in Preventing Catalase Inactivation

Effect of Prostaglandin F2ÃÂ± on Growth of Staphylococcus Aureus Associated with Bovine Mastitis

Common Solvent Toxicity: Autoxidation of Respiratory Redox-Cyclers Enforced by Membrane Derangement

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Effect of Prostaglandin F2ÃÂ± on Growth of Staphylococcus Aureus Associated with Bovine Mastitis